Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aspirin and paracetamol (acetaminophen) are the most commonly used minor analgesics, but their effects on the gastrointestinal tract differ widely. The effects of other nonsteroidal anti-inflammatory drugs (NSAIDs), including phenylbutazone, are intermediate. Aspirin is significantly associated with major upper gastrointestinal haemorrhage, whereas paracetamol is not. Short term use of aspirin produces erythema, erosions and occasionally ulcers; paracetamol does not, while other NSAIDs do so to varying degrees. Chronic gastric ulcer is linked to aspirin intake in patients with rheumatic disease, and epidemiologically in all heavy aspirin users. In only one epidemiological study was a paradoxical significant association reported between paracetamol intake and chronic gastric ulcer. Faecal occult blood loss is increased in most regular aspirin users but not in those taking paracetamol. Although formal studies in children have apparently not been made, in isolated small clinical series it has been reported that gastrointestinal bleeding and anaemia do occur in the paediatric age group after the use of aspirin. Pathophysiologically, aspirin alters the gastric mucosal barrier to hydrogen ions and lowers gastric potential difference; paracetamol has no effect on these parameters. Such changes correlate ultrastructurally with damage in surface epithelial cells and microerosions after the use of aspirin, but not after the use of paracetamol. Aspirin and other NSAIDs cause a dramatic reduction in the ability of gastric mucosa to generate protective prostaglandins; however, paracetamol also reduces prostaglandins. Other postulated mechanisms of aspirin damage include reduction in gastric mucosal secretion, reduction in bicarbonate output, and alteration of cell turnover. Because damage to gastric mucosa by aspirin and NSAIDs is often 'silent', the clinician needs a high level of suspicion and awareness regarding this problem. In patients prone to gastric damage, or in those with a past history of aspirin-induced gastric damage, paracetamol is the drug of choice when a minor, non-inflammatory problem requires an analgesic.
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PMID:Gastrointestinal intolerance and bleeding with non-narcotic analgesics. 355 87

Aspirin and paracetamol (acetaminophen) are the most commonly used minor analgesics, but their effects on the gastrointestinal tract differ widely. Aspirin is significantly associated with major upper gastrointestinal hemorrhage, whereas acetaminophen is not. Short-term use of aspirin produces erythema, erosions, and occasionally ulcers; acetaminophen use does not. Chronic gastric ulcer is linked to aspirin intake in patients with rheumatic disease, and epidemiologically in all heavy aspirin users; paradoxically, in only one epidemiologic study was a significant association found between acetaminophen intake and chronic gastric ulcer. Fecal occult blood loss is increased in most regular aspirin users but not in those taking acetaminophen. Although studies in children have not apparently been made, in isolated small clinical series it has been shown that gastrointestinal bleeding and anemia do occur in the pediatric age group following the use of aspirin. Pathophysiologically, aspirin alters the gastric mucosal barrier to hydrogen ions and lowers gastric potential difference; acetaminophen has no effect on these parameters. Such changes correlate ultrastructurally with damage in surface epithelial cells and microerosions after the use of aspirin, but not after the use of acetaminophen. Aspirin causes a dramatic reduction in the ability of gastric mucosa to generate protective prostaglandins; however, acetaminophen also reduces prostaglandins. Other postulated mechanisms of aspirin damage include reduction in gastric mucosal secretion, bicarbonate output, and alteration of cell turnover. Because aspirin damage to gastric mucosa is often "silent," the clinician needs a high level of suspicion and awareness. In patients prone to gastric damage, or in those with a past history of aspirin-induced gastric damage, acetaminophen is the drug of choice when a minor, noninflammatory problem requires an analgesic.
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PMID:Gastrointestinal effects of antipyretic analgesics. 635 68

Evidences suggest Peroxisome Proliferator Activated Receptor-gamma (PPAR-gamma) ligand, pioglitazone results in the attenuation of gastric mucosal injury. But the molecular mechanism through which these agonists actually elicit gastroprotection through modulating inflammatory responses has not yet been established. Chronic gastric ulcer induced in rats by intraluminal application of acetic acid resulted in elevation of proinflammatory cytokines gene expression, such as, TNF-alpha (Tumor Necrosis Factor-alpha), IL-1beta (Interleukin-1beta) and the protein levels of nuclear p65 subunit of NF-kappaB (Nuclear Factor-kappaB) but decreased levels of PPAR-gamma gene expression. Pioglitazone treatment reduced the severity of ulceration, repressed levels of TNF-alpha, IL-1beta and nuclear p65 subunit as well as increased the abundance of PPAR-gamma in gastric mucosa. Moreover, it significantly upregulated protein levels of glucocorticoid receptor demonstrating its possible involvement in pioglitazone mediated ulcer healing along with PPAR-gamma. Administration of pioglitazone reverted back the decreased levels of both PPAR-gamma and glucocorticoid receptor, resulting in their redistribution to the nucleus from the cytosol in course of ulcer healing. Moreover, pharmacological inhibition of glucocorticoid receptor function by its antagonist (RU486) inhibited pioglitazone mediated downregulation of TNF-alpha and IL-1beta gene expression confirming involvement of glucocorticoid receptor in pioglitazone mediated ulcer healing. Co-immunoprecipitation studies further established association of PPAR-gamma with glucocorticoid receptor during ulcer healing which was enhanced following pioglitazone administration. Thus, the present study is first of its kind bearing direct relevance to the participation of both PPAR-gamma and glucocorticoid receptor and their physical association in influencing amelioration of inflammatory responses during pioglitazone mediated gastric ulcer healing.
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PMID:Involvement of glucocorticoid receptor and peroxisome proliferator activated receptor-gamma in pioglitazone mediated chronic gastric ulcer healing in rats. 1928 8

Gastric cancer is one of the most common malignancies in the world; however, its exact mechanism of development which may be relevant to many factors is still unclear, such as age, diet, Helicobacter pylori infection, smoking, polyps, chronic gastric ulcer and so on. Chronic gastric ulcer is considered as precancerous lesion of gastric cancer. The above-mentioned diseases are usually diagnosed by endoscopy and biopsy. In general, biopsy specimens are usually taken from the edges of lesions, seldom from the base. In patients with chronic gastric ulcer, especially healing or healed benign ulcer, we took the biopsy specimens from both the edges and the base of ulcers in the follow-up. Malignant lesions were found in several cases of chronic gastric ulcer, in which specimens were taken from the base of lesions. Therefore, we hypothesize that biopsy from the base of healing or healed chronic gastric ulcer in the second or third endoscopy may find gastric cancer earlier than traditional biopsy.
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PMID:Biopsy from the base of gastric ulcer may find gastric cancer earlier. 2104 Oct 36